Mature oligodendrocyte apoptosis precedes IGF‐1 production and oligodendrocyte progenitor accumulation and differentiation during demyelination/remyelination

JL Mason, JJ Jones, M Taniike, P Morell… - Journal of …, 2000 - Wiley Online Library
JL Mason, JJ Jones, M Taniike, P Morell, K Suzuki, GK Matsushima
Journal of neuroscience research, 2000Wiley Online Library
We have documented changes in the oligodendrocyte population during demyelinating
insult to the adult CNS. Feeding of cuprizone to adult mice led to apoptotic death of mature
oligodendrocytes followed by profound demyelination of the corpus callosum. A
regenerative response was initiated even during active demyelination. Oligodendrocyte
progenitors have begun to proliferate and then accumulate within the lesion. Many of these
cells may have migrated from the sub‐ventricular zone and fornix before their accumulation …
Abstract
We have documented changes in the oligodendrocyte population during demyelinating insult to the adult CNS. Feeding of cuprizone to adult mice led to apoptotic death of mature oligodendrocytes followed by profound demyelination of the corpus callosum. A regenerative response was initiated even during active demyelination. Oligodendrocyte progenitors have begun to proliferate and then accumulate within the lesion. Many of these cells may have migrated from the sub‐ventricular zone and fornix before their accumulation in the demyelinating corpus callosum. The accumulation of differentiating oligodendrocyte progenitors was followed closely by the reappearance of mature oligodendrocytes and remyelination. Interestingly, an increase in IGF‐1 mRNA was detected at Week 3 through Week 7, suggesting potential involvement in remyelination. Other factors, however, such as PDGF, NT3, FGF, jagged, and notch remained unchanged. These results suggest that the mature oligodendroglial population depleted by apoptosis is replaced by a newly formed oligodendroglial population derived from progenitors; these accumulate and seem to differentiate during remyelination. J. Neurosci. Res. 61:251–262, 2000. © 2000 Wiley‐Liss, Inc.
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